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Article: Clinicopathologic features of hepatitis C virus infection in renal allograft recipients

TitleClinicopathologic features of hepatitis C virus infection in renal allograft recipients
Authors
Issue Date1994
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.com
Citation
Transplantation, 1994, v. 58 n. 9, p. 996-1000 How to Cite?
AbstractThe clinicopathologic features, the natural history, and the prognostic indicators of hepatitis C virus (HCV)-related liver disease in renal allograft recipients have not been well defined. Among 220 renal allograft recipients, 21 were seropositive for HCV RNA, which persisted on prospective follow-up for 40 months. Elevations in alanine aminotransferase and alkaline phosphatase were noted after renal transplantation in 15 (71.4%) and 9 (42.9%) patients, respectively, with 11 (52.4%) showing recurrent or persistent abnormalities. Mortality from liver failure was noted in 1 patient. Persistence of abnormal liver biochemistry was associated with an early onset of biochemical derangement after transplantation, and a longer dialysis duration (P<0.05). HCV-related liver pathology was assessed in 13 patients by histologic scoring with respect to 'hepatitic activity,' 'bile duct damage,' and 'architectural abnormality,' adding up to a 'total' score. Six (46.2%) of 13 initial liver biopsies showed significant chronic liver disease. Liver histology correlated with mean alanine aminotransferase and alkaline phosphatase levels after renal transplantation, and was more severe in patients with persistent biochemical abnormalities. Early onset of abnormal liver biochemistry after transplantation and persistently abnormal biochemistry were independent predictors of worse total and activity scores (P<0.05). Renal transplant recipients demonstrated lower activity scores when compared with nonimmunosuppressed subjects with chronic hepatitis C (P=0.03). HCV RNA was detectable in all 23 liver specimens tested. We conclude that significant, potentially life-threatening liver pathology manifests in about half of renal transplant recipients with chronic HCV infection. Liver histology correlates with the longitudinal biochemical profile. Patients with early onset of biochemical abnormalities and persistently deranged liver biochemistry are at risk of developing severe liver disease.
Persistent Identifierhttp://hdl.handle.net/10722/162030
ISSN
2015 Impact Factor: 3.69
2015 SCImago Journal Rankings: 1.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, TMen_US
dc.contributor.authorWu, PCen_US
dc.contributor.authorLau, JYNen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorLok, ASFen_US
dc.contributor.authorCheng, IKPen_US
dc.date.accessioned2012-09-05T05:16:46Z-
dc.date.available2012-09-05T05:16:46Z-
dc.date.issued1994en_US
dc.identifier.citationTransplantation, 1994, v. 58 n. 9, p. 996-1000en_US
dc.identifier.issn0041-1337en_US
dc.identifier.urihttp://hdl.handle.net/10722/162030-
dc.description.abstractThe clinicopathologic features, the natural history, and the prognostic indicators of hepatitis C virus (HCV)-related liver disease in renal allograft recipients have not been well defined. Among 220 renal allograft recipients, 21 were seropositive for HCV RNA, which persisted on prospective follow-up for 40 months. Elevations in alanine aminotransferase and alkaline phosphatase were noted after renal transplantation in 15 (71.4%) and 9 (42.9%) patients, respectively, with 11 (52.4%) showing recurrent or persistent abnormalities. Mortality from liver failure was noted in 1 patient. Persistence of abnormal liver biochemistry was associated with an early onset of biochemical derangement after transplantation, and a longer dialysis duration (P<0.05). HCV-related liver pathology was assessed in 13 patients by histologic scoring with respect to 'hepatitic activity,' 'bile duct damage,' and 'architectural abnormality,' adding up to a 'total' score. Six (46.2%) of 13 initial liver biopsies showed significant chronic liver disease. Liver histology correlated with mean alanine aminotransferase and alkaline phosphatase levels after renal transplantation, and was more severe in patients with persistent biochemical abnormalities. Early onset of abnormal liver biochemistry after transplantation and persistently abnormal biochemistry were independent predictors of worse total and activity scores (P<0.05). Renal transplant recipients demonstrated lower activity scores when compared with nonimmunosuppressed subjects with chronic hepatitis C (P=0.03). HCV RNA was detectable in all 23 liver specimens tested. We conclude that significant, potentially life-threatening liver pathology manifests in about half of renal transplant recipients with chronic HCV infection. Liver histology correlates with the longitudinal biochemical profile. Patients with early onset of biochemical abnormalities and persistently deranged liver biochemistry are at risk of developing severe liver disease.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.transplantjournal.comen_US
dc.relation.ispartofTransplantationen_US
dc.subject.meshAdulten_US
dc.subject.meshAlanine Transaminase - Blooden_US
dc.subject.meshAlkaline Phosphatase - Blooden_US
dc.subject.meshBiopsyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHepacivirus - Isolation & Purificationen_US
dc.subject.meshHepatitis C - Etiology - Metabolism - Pathologyen_US
dc.subject.meshHepatitis, Chronic - Etiology - Metabolism - Pathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshKidney Transplantation - Adverse Effectsen_US
dc.subject.meshLiver - Enzymology - Pathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshProspective Studiesen_US
dc.subject.meshRna, Viral - Analysisen_US
dc.subject.meshTransplantation, Homologous - Adverse Effectsen_US
dc.titleClinicopathologic features of hepatitis C virus infection in renal allograft recipientsen_US
dc.typeArticleen_US
dc.identifier.emailChan, TM:dtmchan@hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityChan, TM=rp00394en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1097/00007890-199411150-00004-
dc.identifier.pmid7974739-
dc.identifier.scopuseid_2-s2.0-0028032375en_US
dc.identifier.hkuros5580-
dc.identifier.volume58en_US
dc.identifier.issue9en_US
dc.identifier.spage996en_US
dc.identifier.epage1000en_US
dc.identifier.isiWOS:A1994PR96400004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChan, TM=7402687700en_US
dc.identifier.scopusauthoridWu, PC=7403119323en_US
dc.identifier.scopusauthoridLau, JYN=7402446047en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridLok, ASF=35379868500en_US
dc.identifier.scopusauthoridCheng, IKP=7102537483en_US

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